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Despite improvements in diagnostic methods and the introduction of new imaging methods, neither plaque rupture nor plaque erosion can be predicted in clinical practice. Inflammation at the site of plaque rupture or erosion is an important determinant of plaque instability [1]. Activated macrophages either weaken the overlying fibrous cap of plaques, thereby leading to plaque rupture, or promote thrombosis and vasoconstriction in nonruptured but inflamed plaques. It has been suggested that measurement of temperature released by activated inflammatory cells of atherosclerotic plaques may detect plaque instability. Previous ex vivo studies have shown that there is thermal heterogeneity in human carotid atherosclerotic plaques [2].